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Personal profile

Biography

Dr Pearson moved from Perth to Melbourne in 2009 to complete a PhD at The University of Melbourne. She was awarded an NHMRC Early Career Fellowship in 2014 and has recently been appointed laboratory head within the Centre for Innate Immunity and Infectious Diseases at The Hudson Institute of Medical Research.

Over the past 7 years, Dr Pearson has worked towards understanding how bacterial virulence or “effector” proteins injected by gut pathogens shut down host immune responses to avoid clearance and cause disease.  She has made several key discoveries showing that disease-causing E. coli specifically target and inhibit programmed cell death pathways (apoptosis and necroptosis) in the host, allowing persistence of the pathogen. Overall her work has led to the identification of host responses that are essential for controlling bacterial infections of the gut and maintaining gut homeostasis.

Dr Pearson’s previous research on E. coli pathogenesis has fuelled a new interest in understanding disease mechanisms of the foodborne pathogen Salmonella. Pathogenic serovars of Salmonella are the causative agents of a spectrum of disease states, including typhoid fever, self-limiting gastroenteritis, and invasive bacteremia. In Australia, disease caused by Salmonella enterica serovar Typhimurium is on the rise, with over 18, 000 notifications nationally in 2016. Her current research is focused on understanding the role of programmed cell death in Salmonella infections in vivo.

The manipulation of host immune responses by some bacteria is a phenomenon shared with many viruses, thus Jaclyn also has a keen interest in understanding bacterial-viral interactions in the gut and the implications for disease outcomes.

Overall, Dr Pearson’s research program aims to address mechanisms of disease caused by gut pathogens and inflammatory diseases caused by dysregulated immune responses in the gut.

Keywords

  • Salmonella
  • Necroptosis
  • Cell death
  • Inflammation
  • Type III effector proteins
  • Apoptosis
  • Gut pathogens
  • Inflammatory bowel disease
  • Innate immunity

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Projects 2018 2022

Research Output 2011 2017

Distinct roles of the antiapoptotic effectors NleB and NleF from enteropathogenic Escherichia coli

Pollock, G. L., Oates, C. V. L., Giogha, C., Lung, T. W. F., Ong, S. Y., Pearson, J. S. & Hartland, E. L., 1 Apr 2017, In : Infection and Immunity. 85, 4, 12 p., e01071-16.

Research output: Contribution to journalArticleResearchpeer-review

EspL is a bacterial cysteine protease effector that cleaves RHIM proteins to block necroptosis and inflammation

Pearson, J. S., Giogha, C., Mühlen, S., Nachbur, U., Pham, C. L. L., Zhang, Y., Hildebrand, J. M., Oates, C. V., Lung, T. W. F., Ingle, D. J., Dagley, L. F., Bankovacki, A., Petrie, E. J., Schroeder, G. N., Crepin, V. F., Frankel, G., Masters, S. L., Vince, J., Murphy, J. M., Sunde, M. & 3 othersWebb, A. I., Silke, J. & Hartland, E. L., 13 Jan 2017, In : Nature Microbiology. 2, 16258.

Research output: Contribution to journalArticleResearchpeer-review

Host Innate Immune Factors Influencing Enterohemorrhagic Escherichia coli Pathogenicity

Zhang, Y., Pearson, J. S. & Hartland, E. L., 2017, Foodborne Pathogens : Virulence Factors and Host Susceptibility. Gurtler, J. B., Doyle, M. P. & Kornacki, J. L. (eds.). Cham, Switzerland: Springer, p. 355-373 19 p.

Research output: Chapter in Book/Report/Conference proceedingChapter (Book)Otherpeer-review

The type III effector NleD from enteropathogenic Escherichia coli differentiates between host substrates p38 and JNK

Creuzburg, K., Giogha, C., Lung, T. W. F., Scott, N. E., Mühlen, S., Hartland, E. L. & Pearson, J. S., 2017, In : Infection and Immunity. 85, 2, e00620-16.

Research output: Contribution to journalArticleResearchpeer-review

Identification of a distinct substrate-binding domain in the bacterial cysteine methyltransferase effectors NleE and OspZ

Zhang, Y., Mühlen, S., Oates, C. V., Pearson, J. S. & Hartland, E. L., 16 Sep 2016, In : Journal of Biological Chemistry. 291, 38, p. 20149-20162 14 p.

Research output: Contribution to journalArticleResearchpeer-review